Lysosomes and tegument pathology in the chemotherapy of schistosomiasis with 1,7-bis(p-aminophenoxy)heptane (153C51).

One therapeutic oral dose (400 mg/kg) of 153C51 administered to infested mice caused pathological changes in the dorsal region of the tegument of male Schistosoma mansoni during the period 3--24 h after treatment. These changes occurred prior to the 'hepatic shift'. At the ultrastructural level they consisted of a gradual accumulation in the tegument epidermis of numerous membranous inclusions with the characteristics of residual lysosomes and changes in the localization of acid phosphatase, a lysosomal enzyme. It seemed likely that these changes were due to inhibition or exhaustion of enzyme in the epidermis, followed by re-synthesis of enzyme in the cell bodies and its export to the epidermis. The elimination of hydrolytic activity from lysosomes in the epidermis would explain the accumulation of residual lysosomes. Drug-treated parasites retained their disguise of host red blood cell ghost antigens as shown by indirect fluorescent antibody-labelling and, therefore, it seemed unlikely that immunological factors could be important in producing the tegument pathology.